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RV FRCERV=−
FR
Initial helium concentration)
Final helium concentration)
(
(
VV
F
F
A
=−
8
7
Litres
Time
Total lung capacity
6
volume
5
4
3
2
1
0
Expiratory
reserve
volume
reserve
Inspiratory
Fig. 8.6 Normal adult lung volumes.
Tidal
volume
Residual
volume
CHAPTER 8 Respiratory System
capacity
Inspiratory
Functional residual
capacity
Vital
capacity
capacity
Expiratory
191
• residual volume (RVol): the volume remaining aer
maximal expiration; it cannot be measured directly
but can be estimated from other lung volumes:
• e anatomical dead space can be determined using
Fowler’s method (Fig. 8.7). e subject breathes through
a tube connected to a nitrogen analyser. e subject
takes a single breath of pure oxygen, holds the breath for
several seconds and then breathes out. By performing
this manoeuvre the composition of air within the alveoli
• total lung capacity (TLC): the sum of all lung volumes plus the residual volume
• vital capacity (VC): the volume of air that is expelled
from maximal inspiration to maximal expiration.
• Normal spirometry traces are shown in Fig. 8.6; they
may vary for size, weight and gender.
• e FRC can be determined by the helium dilution
method. e subject breathes normally from a spirometer lled with a known volume of air and helium. As the
subject breathes in and out the helium is diluted in the air
that is le in the lungs:
will dier from that within the airways (i.e. alveoli will
contain nitrogen but airways higher up will have pure
oxygen).
• Subject breathes out pure O2 (from conducting airways).
• As subject starts to expire, the nitrogen content of alveolar air is measured.
• A plot of exhaled volume to nitrogen concentration is
produced; the dead space is the volume at the midpoint
between nitrogen rst being detected and its plateau.
• Physiological dead space can be determined from the
Bohr equation.
• e principles of this equation rely on two facts:
volume of spirometer
×
C
=
• all of the expired CO2 comes from the alveoli
• dead space is atmospheric air and thus has negligible
CO2 content.
• e RV can be calculated by the same method, but the
subject takes a maximal expiration (i.e. only RV in the
lungs) before breathing from the spirometer.
Dead Space and Alveolar Ventilation Rate
• Dead space is the volume of air which has to be ventilated, but does not actually take part in gas exchange.
• Dead space can be anatomical or physiological:
• anatomical dead space is the volume of gas that does
not mix with the air in the alveoli
• physiological dead space is the volume of gas that
may reach the alveoli but, due to a lack of perfusion,
does not take part in gas exchange (this includes air
in the anatomical dead space).
• e Bohr equation is:
E
1
DE
VD: volume of dead space
VE: volume of expired CO
FE: fraction of expired CO
FA: fraction of alveolar CO
• FE can be measured simply by measuring the CO2 con-
2
2
2
tent of expired air.
• FA can be measured from:
• the last part of the expired air, which will have the
same composition as alveolar air
• arterial blood gas (more accurate).
192
V
V
D
=−
=
35
.
Alveolar ventilation rate TV dead space
=−
()
()
.
=
42 L/min
EXP
Vol. expired (mL)
% N
0
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SECTION II Physiology
100
2
50
200
Mid-point
150
100
Vol. of dead space
Fig. 8.7 Fowler’s method for determination of the anatomical dead space.
• For a normal subject with a tidal expiration of 500 mL,
expired CO2 = 3.5% and alveolar CO2 = 5%; the dead
space:
500 1
D
50
.
mL
500
• Factors that increase anatomical and physiological dead
space are given in Table 8.2.
TABLE 8.2 Factors Increasing Anatomical
and Physiological Dead Space
Anatomical Dead Space
Increasing size of the subject Hypotension
Standing position Hypoventilation
Increased lung volume Emphysema
• Alveolar ventilation rate is the rate at which gas in the
alveoli is replaced:
Respiratoryrate
×
()
=−×
500150 12
RR
Bronchodilatation Positive pressure
• Values will fall dramatically in respiratory disease; PEFR
is particularly useful in assessing the severity of acute
asthma attacks.
Peak Expiratory Flow Rate (PEFR)
• A simple bedside test of respiratory function.
• Patient is asked to take maximal inspiration and then to
blow out as fast as possible into the peak ow meter.
• Values will vary for age, sex and weight, but a value of
around 4–500 L/min is normal.
Closing Capacity
• is is the volume of the lungs at which small airways at
the base of the lung start to close.
• e signicance of the closing capacity is that as air
leaves the lungs some airways close and trap air in the
Physiological Dead
Space
and PE
ventilation
CHAPTER 8 Respiratory System
Lung vol. (L)
100
1 2 3 4
2
% N
Closing
capacity
TLC FRC CC RV
Fig. 8.8 The concentration of nitrogen following a single inspiration of 100% oxygen. The closing capacity is
indicated at the point of abrupt increase in the nitrogen concentration.
193
alveoli; these alveoli cannot play a full part in respiratory gas exchange.
• Closing capacity can be measured by the following
technique:
• the subject breathes out to residual volume and then
takes a maximal inspiration of 100% O
• the subject then takes a full expiration through a
2
nitrogen meter
• the plot of nitrogen concentration to lung volume
gives a characteristic plot with four phases (Fig. 8.8):
• phase 1: pure dead space is exhaled and is therefore 100% O
• phase 2: mixture of dead space and alveolar gas
2
(nitrogen concentration from alveoli increases
concentration)
• phase 3: pure alveolar gas (plateau phase)
• phase 4: abrupt increase in nitrogen concentration as airways at the base of the lung close.
Expired air at this point is from the apex, which
has received less O2, and thus the nitrogen is less
dilute.
• Closing capacity is normally 10% of the vital capacity.
• Factors aecting the closing capacity include:
• age: increases with age
• posture: in a supine position in a 40-year-old subject,
the closing capacity is equal to the FRC
• anaesthesia: decrease in lung volumes results in closing capacity exceeding FRC, even in the youngest
patients.
Flow–Volume and Volume–Time Curves
• Spirometry values should always be assessed with ow–
volume and volume–time curves. Diseases of the lung
produce characteristically shaped curves.
• Flow–volume curves (Fig. 8.9).
• Volume–time curves (Fig. 8.10).
Diffusion Capacity
• Diusion capacity (DLCO) or transfer factor (TLCO) is a
test that reects both the diusion capacity of the alveolar membrane and also the pulmonary vasculature.
• It can be measured by inhaling very small concentrations of carbon monoxide and measuring the increase
in arterial CO.
• DLCO is reduced with:
• ↑ in diusion distance, i.e. pulmonary oedema
• loss of alveolar area, i.e. emphysema.
PULMONARY BLOOD FLOW
Structure of the Lung
See Anatomy section (Chapter 1).
194
Vol (L)
Vol (L)
Flow (L/s)
TLC RV
Vol (L)
Volume
Time
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SECTION II Physiology
Flow (L/s)
Normal
Restrictive
Normal
Normal
A
Flow (L/s)
B
C
Fig. 8.9 (A) A normal flow–volume curve. (B) An
obstructive defect with characteristic concave shape
during expiration. (C) The relatively unaffected shape
but significantly decreased volume seen in restrictive lung disease.
TLC RV
Obstructive
TLC RV
Restrictive
Obstructive
1
FVCFEV
Fig. 8.10 FEV1/FVC ratios. Normal = 4 L/5 L = 80%.
Obstructive FEV1/FVC = 1.2/3 = 40%. Restrictive FEV1/
FVC = 2.9/3.2 = 93%. FEV1, Forced Expiratory Volume
in the first second; FVC, Forced Vital Capacity.
Regulation of Pulmonary Blood Flow
• Pulmonary arterioles do not appear to play an important
role in the regulation of pulmonary blood ow, but the calibre of small alveolar vessels is altered by the PO2 and PCO2.
• Hypoxia (↓PO2) or hypercapnia (↑PCO2) result in constriction of vessels and thus divert blood to areas that
are better oxygenated; this is termed hypoxic pulmonary vasoconstriction (HPV).
• is is a local response and diers from other vascular
beds in that the opposite response is usually seen (i.e.
hypoxia causes vasodilatation).
Regional Variations in Pulmonary Blood Flow
• Perfusion pressure and resistance determine ow.
• Pressure in the pulmonary artery is low in comparison
with the systemic circulation: 25/8 mmHg compared
with 120/80 mmHg.
• Blood ow in the lung is determined by three pressures:
• hydrostatic pressure in the pulmonary arteries (PA)
• pressure in the pulmonary veins (PV)
• pressure of air in the alveoli.
• With these forces in mind the blood ow to the lung can
be divided into three zones:
• zone 1: this is at the apex of the lung; the alveolar
pressure is similar to the PA pressure; smaller vessels
will be compressed and resistance will be high. Blood
ow is low in this zone
CHAPTER 8 Respiratory System
195
• zone 2: pressure in the PA is higher than the alveolar
pressure; blood ow is better in this zone, increasing
towards zone 3
• zone 3: PA pressure greatly exceeds the alveolar pressure and thus vessels are fully open. Blood ow is
very good.
• e variations in regional blood ow are abolished on
lying down.
Cardiac Output and Pulmonary Vascular
Resistance
• During exercise the CO to the lungs increases but the
pressure within the PA changes relatively little; this is
due to two mechanisms which decrease resistance when
CO increases:
• distension of vessels already open
• recruitment of additional vessels (at rest many capil-
laries are closed).
• e response to the increase in CO is passive.
Ventilation and Perfusion
• Ventilation and perfusion (V/Q) varies throughout the
lung, depending on the height above or below the origin
of the PA.
• e V/Q ratio expresses this variation:
• in alveoli that are ventilated but not perfused V/Q =
innity
• in alveoli that are perfused but not ventilated V/Q = 0
• at the apex V/Q = 3, thus indicating that the alveoli
are ventilated better than they are perfused
• at the base V/Q = 0.6, thus indicating that the alveoli
are perfused better than they are ventilated
• the ideal V/Q = 1 and is found approximately two-
thirds of the way up the chest
• the average V/Q ratio, assuming an alveolar ventila-
tion rate of 4.2 L/min, and a cardiac output of 5 L/min,
would be 0.84.
Clinical Physiology
Pulmonary Embolus
• A pulmonary embolus results from a thrombus breaking o from a thrombus formed in the large leg/pelvic
veins; this clot then lodges in the pulmonary arteries.
• A pulmonary embolus can also occur with fat, amniotic
uid, air or tumour fragments; these are all very rare.
• e eect of the embolus will depend on its size: clinical
presentation varies from complete obstruction and sudden death, to the insidious development of hypoxia due
to numerous small emboli.
• e physiological changes associated with a pulmonary
embolus include:
• increased pulmonary vascular resistance
• pulmonary hypertension
• increased right ventricle (RV) aerload (leading to
RV dilatation and dysfunction)
• reduced le ventricle output
• impaired gas exchange, due to shunting of blood
through non-perfused segments of lung
• decreased lung compliance, due to bleeding and loss
of surfactant over the area aected by the embolus.
Pleural Effusion
• is refers to the abnormal presence of uid within the
pleural cavity.
• e physiological consequences are similar to those of
pneumothorax, i.e. hypoxia occurs as lung tissue is compressed by the uid and prevents normal gas exchange.
• e uid can be classied as a transudate or an exudate:
• an exudate has a high protein content (>30 g/L) and
is usually due to infection or cancer
• a transudate has a low protein content (<30 g/L) and
most commonly is due to le ventricular failure.
Pulmonary Oedema
• Pulmonary oedema is the abnormal accumulation of
uid in the lung parenchyma.
• Starling’s law states that hydrostatic forces push uid out
of the circulation and osmotic forces draw uid back.
• Normally the balance of hydrostatic and osmotic forces
leads to 20–30 mL of excess uid in the lung interstitium; this is transported back to the circulation as
lymph.
• Pulmonary oedema occurs in stages:
• interstitial oedema: this has little eect on respira-
tion, but will eventually overwhelm lymphatic recirculation and lead to alveolar oedema
• alveolar oedema: as alveolar oedema develops, the
alveoli ll with uid; this increases surface tension
and causes the alveoli to shrink
• airway oedema: as uid accumulation continues
then uid will begin to ll the airways; this presents
as blood-tinged frothy sputum.
• e physiological eects of pulmonary oedema include:
• decreased lung compliance due to the reduction in
surface tension and alveolar shrinkage
• increased airway resistance: this can occur due to the
reduction in lung volume and uid lling the airways.
Resistance is also due to reex bronchoconstriction.
• Alveolar oedema leads to a ventilation–perfusion mismatch as alveoli lled with uid are still perfused but
not ventilated.
• Pulmonary vascular resistance increases due to hypoxic
vasoconstriction and external compression from interstitial oedema.
196
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SECTION II Physiology
• ere are numerous causes of pulmonary oedema; these
include:
• raised pulmonary hydrostatic pressure, the com-
monest cause, occurs with le ventricular failure –
le atrial pressure rises and this is transmitted into
the pulmonary circulation, resulting in increased
pulmonary capillary pressure, and thus capillary
hydrostatic pressure. is type of pulmonary oedema
can also be seen with uid or transfusion overload
• increased pulmonary capillary permeability: this can
occur with endotoxic shock, irritant gases and adult
respiratory distress syndrome (ARDS)
• blocked lymphatic drainage: this can occur in the face
of normal pulmonary hydrostatic pressures and normal capillary permeability. e commonest cause is
obstruction of lymphatics due to tumour cells. e normal 20–30 mL of interstitial uid normally removed
by lymphatics accumulates and leads to pulmonary
oedema – it is called lymphangitis carcinomatosa
• high altitude: the exact cause is unclear, but is likely
to be due to hypoxic vasoconstriction leading to
elevated pulmonary artery pressure and thus an
increase in the hydrostatic pressure
• neurogenic: frequently seen in severe head injury
patients, it is thought to occur due to overactivity of
the sympathetic nervous system.
Adult Respiratory Distress Syndrome
• ARDS is the pulmonary component of the systemic
inammatory response syndrome (SIRS).
• It can be caused by direct (contusion, near drowning,
aspiration, smoke inhalation) or indirect (trauma, sepsis, pancreatitis) insults.
• Criteria for its diagnosis include:
• known cause
• acute onset of symptoms
• hypoxia refractory to O
• new, bilateral ‘uy’ inltrates on chest X-ray
2
• no evidence of cardiac failure (pulmonary artery
wedge pressure <18 mmHg).
• ARDS develops in two phases:
1. acute exudative: the insult (direct or indirect) leads
to neutrophil activation and the release of inammatory mediators such as tumour necrosis factor
(TNF), platelet activating factor (PAF), interleukin
(IL)-1 and IL-6; there is also the release of proteases and toxic oxygen radicals that damage the lung
parenchyma. is lung damage leads to increased
capillary permeability and allows protein-rich exudates to ll the alveoli and form hyaline membranes.
ere is thrombosis in alveolar capillaries and
haemorrhage into the alveoli. is leads to alveolar
collapse and decreased surfactant production, leading to decreased lung compliance
2. late organization: there is regeneration of type II
pneumocytes; the hyaline membranes organize with
pulmonary brosis, leading to interstitial brosis
and obliteration of alveolar spaces and alveolar
microvasculature.
Gas Diffusion and Exchange
Gas Diffusion
• ree factors aect the diusion of gases, both in the
lungs and in the peripheral tissues:
• pressure gradient: gas ows from an area of high
pressure to an area of low pressure. is is usually
referred to as the partial pressure
• diusion coecient: a measure of the ease with
which a gas can diuse. It is determined by its solubility in water and its molecular weight
• tissue factors: the tissue at the site of diusion should
have a large surface area and a short diusion distance. e surface area of the lungs is about 70 m2
and the diusion distance is 0.2 µm.
• e diusion distance for oxygen consists of:
• pulmonary surfactant
• alveolar epithelium
• alveolar epithelium basement membrane (BM; oen
fused with capillary BM)
• pulmonary capillary endothelium.
Gas Exchange (Table 8.3)
• e exchange of gases in both peripheral tissues and
alveoli relies on partial pressure gradients. In alveoli the
gradient is between alveolar gas and pulmonary blood
gas, while in the periphery the gradient is between capillary blood and metabolically active tissues.
• Room air: mixture of nitrogen and oxygen, water vapour
(variable) and a tiny amount of carbon dioxide.
• Humidied air: inspired air becomes fully saturated
with water; the partial pressure of water vapour is
6.3 kPa; the addition of water vapour leads to a decrease
in the partial pressures of all other gases.
• Alveolar air: diers from room air due to the addition of
water vapour and the constant removal of oxygen and
carbon dioxide i.e. oxygen levels are lower and carbon
dioxide levels are higher in comparison to room air.
Gas Transport (Fig. 8.11)
• Systemic venous blood is pumped into the pulmonary
artery from the right ventricle. PO2 is 5.3 kPa and PCO2 is
6 kPa. Alveolar PO2 is 13.7 kPa and the PCO2 is 5.3 kPa.
• Following the principle of gases owing from areas of
high partial pressure to low partial pressure, oxygen will
Pulmonary
Pulmonary
CHAPTER 8 Respiratory System
TABLE 8.3 Standard Values for Respiratory Gases
Gas Room Air (kPa) Humidified Air (kPa) Alveolar Air (kPa)
N
O
CO
2
2
2
79.79 74.83 75.6
21.17 19.87 13.7
0.04 0.04 5.3
H2O 0 6.3 6.3
Total 101 101 101
Oxygen transport
• Haemoglobin:
• consists of four peptide chains; two α and two β.
Each peptide has a haem group which consists of
a protoporphyrin ring surrounding a ferrous iron
molecule (Fe2+)
• each haemoglobin (Hb) molecule can carry four
oxygen molecules
• normal Hb values for a male and female are 15 g/dL
and 13 g/dL, respectively. Each gram of Hb can carry
artery
PO
PCO
2
2
= 13.7
= 5.3
CO
2
O
PO
PCO
Alveoli
2
PO
PCO
2
2
= 13.7
= 5.3
vein
= 5.3
2
= 6
2
1.34 mL of O2; therefore, O2-carrying capacity varies
between 20 and 17.5 mL per 100 mL blood
Right
heart
Left
heart
• the vast majority of O2 is transported via Hb; only a
negligible amount is dissolved, approximately 0.225
per kPa of O2.
• Oxygen dissociation curve (Fig. 8.12):
• the oxygen dissociation curve illustrates the relation-
Systemic
vein
PO
PCO
2
= 5.3
2
= 6
PO
PCO
= 13
2
= 5.3
2
Systemic
artery
ship between the partial pressure of O2 and the concentration of O2 in the blood
• the characteristic shape of the curve reects the
increasing ability of Hb to take up O2 following the
binding of the rst molecule
Fig. 8.11 The gas exchange between the lungs and
tissues.
• the curve reaches a plateau at a PO2 of around 15–16
kPa
• a number of factors will alter the position of the
curve. A right shi decreases oxygen anity and
diuse into the blood and carbon dioxide will diuse
into the alveoli.
• Oxygenated blood is returned to the heart via the pulmonary veins and then to the le ventricle.
• PO2 of systemic blood is slightly lower than pulmonary
venous blood, due to the addition of deoxygenated
blood from bronchial veins (13.7 kPa → 13 kPa).
• e deoxygenated blood from bronchial veins is
referred to as ‘shunting’; it describes the passage of
blood through the lungs without coming into contact
with ventilated alveoli. Other causes of shunt include:
• pneumonia (due to consolidation of lung parenchyma)
• atrial septal defect
• ventricular septal defect
• patent ductus arteriosus.
thus oxygen will be released at a higher partial pressure. A le shi increases oxygen anity
• a right shi is caused by:
• ↑temperature
• ↑2,3-diphosphoglycerate (2,3-DPG)
+
• ↑H
• the right shift of the dissociation curve is called
the Bohr effect; the factors causing a right shift
would be present in active tissues; the Bohr
effect represents a mechanism to increase oxygen
extraction
• anaemia does not aect the dissociation curve. e
shape and position are the same; to see the eect
of anaemia you would need to plot partial pressure
against oxygen content.
197
198
100
Saturation (%)
13
100
O
saturation (%)
020406080 100 120
(mmHg)
Myoglobin
O
saturation (%)
)
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SECTION II Physiology
90
80
70
60
50
40
30
20
10
0
01234
A
75
50
2
25
0
0
246810 12 14 16
B
PCO
2,
2,3-DPG
TºC
[H+]
5
7
6
PaO2 (kPa)
PO
2
(kPa)
8910 11 12
100
75
50
2
25
0
0
C
0
Fetal Hb
Adult Hb
PO
2
2468
20 40 60 80 100120 (mmHg
10 12 14 16
(kPa)
Fig. 8.12 (A) Oxyhaemoglobin dissociation curve. (B) Factors that shift the oxyhaemoglobin curve to the right
and increase O2 dissociation. (C) Different O2 affinities for fetal haemoglobin and myoglobin in comparison
with the O2 dissociation curve for adult Hb.
• Fetal haemoglobin and myoglobin:
• fetal haemoglobin (HbF) has dierent globin chains
to adult Hb (two α and two γ); the change in globin
chain results in a greater anity for O2 and allows the
fetus to extract blood from the maternal circulation
• the curve for HbF is to the le of adult Hb, reecting
the increased anity for O
• the curve for myoglobin lies further to the le; it acts
as an oxygen storage molecule and only releases O2
when the partial pressure has fallen considerably
• the function of myoglobin is to provide additional O2
in muscles during periods of anaerobic respiration
(i.e. during sustained contractions when blood vessels are compressed).
2
Carbon dioxide transport
• Carbon dioxide is transported in three main ways:
• carbamino groups: these are formed between CO2
and proteins or peptides. Most of these reactions are
with the globin portions of haemoglobin, accounting
for 20–30% of transported CO
• dissolved CO2 accounts for about 10% of the transported CO
• HCO
ported CO2. e CO2 diuses into the red blood cells
2
−
accounts for about 60–70% of the trans-
3
2
and reacts with water to form carbonic acid (a reaction catalysed by the enzyme carbonic anhydrase).
e carbonic acid dissociates into H+ and HCO
the H+ binds to haemoglobin and the HCO
−
diuses
3
−
;
3
30
60
Low (venous) PO
40 50 60 (mmHg)
55
blood)
–1
50
contents (ml 100 mL
2
45
CO
40
4
Y
High (arterial) PO
X
567
Fig. 8.13 The CO2 dissociation curve – Haldane effect.
X indicates CO2 content in systemic arterial blood (↑O2)
and Y indicates CO2 content in venous blood (↓O2).
out of the cell into the plasma. To maintain cellular
balance Cl− diuses into the red cell (chloride shi).
is process is reversed in the alveoli, producing
CO2 in preparation for expiration.
• e CO2 dissociation curve is for total CO2 and not one
form; there are several dierences between it and the
oxygen dissociation curve (Fig. 8.13):
• the solubility of CO2 is greater than oxygen
• the normal range of CO2 is much smaller: 5.3–6 kPa
compared with 5.3–13.3 kPa for oxygen
• blood cannot be saturated with CO2, therefore the
graph has no plateau phase.
• e CO2 dissociation curve is inuenced by the partial
pressure of O2. Essentially the amount of carbon dioxide
carried increases as the oxygen level falls; this eect is
called the Haldane eect.
• e signicance of the Haldane eect is that as arterial blood (PCO2 5.3 kPa) passes through the capillary
network (PCO2 6 kPa), the dissociation curve moves
upwards and allows the increased uptake of CO2.
Regulation of Respiration
e body maintains the amount of PO2 and PCO2 at appropriate levels through an interaction between neurological
and chemical control mechanisms.
Neurological Regulation
• ere are a number of areas in the brain that exert differing degrees of control on respiration. These areas
include:
• medulla oblongata
Pco
8
CHAPTER 8 Respiratory System
199
• pons
2
• cerebral cortex
• limbic system and hypothalamus.
• Medulla oblongata: there are two groups of cells within
the respiratory centre in the medulla:
• the inspiratory neurons: these demonstrate rhythmi-
2
cal ring of action potentials with intervening periods of inactivity. ese action potentials stimulate
the diaphragm and external intercostals to contract,
and thus initiate inspiration. Expiration occurs during the intervening pauses of inactivity
• the expiratory neurons: these neurons are usually
2
(kPa)
inactive during normal quiet respiration; however,
during periods of exercise or increased respiration
they re action potentials during the inactive period
of the inspiratory neurons to stimulate the internal
intercostals and abdominal muscles to contract, and
thus aid expiration.
• Pons: there are two areas within the pons; they are not
essential for respiration, but can inuence the pattern of
breathing:
• apneustic centre: this is located in the lower pons;
it tends to prolong inspiration and results in short
expiratory eorts
• pneumotaxic centre: this is located in the upper
pons; it tends to inhibit the inspiratory neurons and
shortens inspiration.
• Cerebral cortex: this can override the neurons within
the medulla and increase ventilation (hyperventilate) or
hold the breath.
• Limbic system and hypothalamus: in extreme states of
emotion, such as fear or anger, these areas may inuence the respiratory pattern.
Chemical Regulation
• e rhythmical ring of neurons in the medulla is regulated by the input of a number of chemoreceptors, which
monitor changes in chemical factors and then signal the
medulla to increase or decrease the respiratory rate to
normalize the detected chemical change.
• ese chemoreceptors monitor changes in the following:
• arterial PCO
• arterial pH
2
• arterial PO2.
• ese chemoreceptors can be further subdivided into:
• central chemoreceptors
• peripheral chemoreceptors.
• Central chemoreceptors:
• situated in the CNS, close to the respiratory centre in
the medulla
• particularly sensitive to changes in the arterial
PCO
2
200
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SECTION II Physiology
• CO2 diuses from the blood into the brain and reacts
with water to produce H+ and causes the pH to fall,
thus directly stimulating the chemoreceptors
• any elevation in CO2 leads to a central acidosis
that stimulates the chemoreceptors and leads to an
increased respiratory rate in order to blow o the
excess CO2. e opposite eect is seen with low levels of CO
• central chemoreceptors are the main determinant of
2
respiration, as the level of CO2 is the most important
stimulus to respiration.
• Peripheral chemoreceptors:
• located in the carotid bodies, close to the bifurcation of the common carotid and in the aortic bodies,
which lie along the aortic arch
• less important than the central chemoreceptors
• they respond to changes in arterial pH and to low
levels of PO2; the response to pH is of secondary
importance to respiratory control but does allow
compensation for acid–base disturbances
• for instance, a fall in arterial pH due to a metabolic
acidosis will stimulate respiration and thus will lower
the level of CO2 and favour an increase in pH back
towards normal. e opposite eect is seen with an
alkalosis
• the response to low O2 only comes into eect when
levels are abnormally low, i.e. PO2 8 kPa or less
• these receptors can become important in severe
longstanding lung disease with persistently elevated
levels of CO2. Patients may become accustomed and
lose the controlling inuence of CO2. ey therefore
rely on the low level of O2 to stimulate respiration.
is is called hypoxic drive.
• ere are several other factors which may inuence
respiration:
• Hering–Breuer reex: this reex prevents over-ina-
tion of the lungs. Stretch receptors in the lung send
inhibitory signals via the vagus. Only signicant at
high tidal volumes (>1.5 L)
• ‘J’ receptors: these receptors lie in the alveoli in close
association with the capillaries. eir function is
unclear but injection of chemicals into the pulmonary circulation triggers these receptors and causes a
marked inhibition of inspiration
• irritant receptors: lie in the epithelia lining the air-
ways; they respond to noxious gases and cause bronchospasm and inhibition of inspiration
• vasomotor centre: low blood pressure detected by
baroreceptors results in an increase in the ventilatory
rate. An increase in blood pressure has the opposite
eect.
Hypoxia and Respiratory Failure
Hypoxia and Hypoxaemia
• Hypoxia: a deciency of oxygen in the tissues.
• Hypoxaemia: reduction in the concentration of oxygen
in the arterial blood.
• ere are four types of hypoxia:
1. Hypoxic hypoxia: results from a low arterial PO2;
examples include:
• high altitude
• pulmonary embolism
• hypoventilation
• lung brosis
• pulmonary oedema.
2. Anaemic hypoxia: a decrease in the amount of hae-
moglobin and thus a decrease in oxygen content of
arterial blood; examples include:
• haemorrhage
• decreased red cell production
• increased red cell destruction
• carbon monoxide poisoning.
3. Stagnant hypoxia: due to low blood ow; examples
include:
• vasoconstriction
• decreased cardiac output: due to the low blood
ow there is increased extraction of oxygen from
the blood; this leads to very low venous oxygen
and produces peripheral cyanosis.
4. Histotoxic hypoxia: poisoning of the enzymes
involved in cellular respiration. Oxygen is available
but cannot be utilized; the main example is cyanide
poisoning.
• ere are ve main causes of hypoxaemia:
1. Hypoventilation, accompanied by ↑PaCO2; oxygen
therapy can improve the hypoxaemia; common
causes of hypoventilation include:
• central depression of respiratory drive, e.g. drugs
• trauma, i.e. cervical cord injury
• neuromuscular disorders, e.g. myasthenia
gravis
• chest wall deformity.
2. Impaired diusion: PaCO2 is usually normal due
to its increased solubility; oxygen therapy can also
improve the hypoxaemia. Causes of impaired diusion include:
• asbestosis
• sarcoidosis
• ARDS.
3. Shunt (see Gas Transport section): PaCO2 is usually
normal, but unlike other causes of hypoxaemia the
administration of oxygen will not raise the PaO2; this
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